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Category Archives: Symptomatic Bradycardia

Question: In the Symptomatic Bradycardia Medical Directive, both atropine administration and TCP have hypothermia listed in the contraindications. However, this contraindication is not present for dopamine administration.

This seems to contradict the practice of not giving drugs to the severely hypothermic patient and focusing prehospital care on rapid transport and passive rewarming. Was this omission voluntary and if so, what is the rationale or the studies that support the use of dopamine in such a case? Thank you!

PS: Hypothermia is not listed as a contraindication for dopamine in the ROSC protocol either.

Answer: Thanks for the very interesting question! To be frank, we are not sure why the contraindications list hypothermia for Atropine and Transcutaneous Pacing (TCP) but do not list hypothermia as a contraindication for Dopamine administration. We will be bringing this back up this Fall when the entire ALS-PCS is opened for revision pending the 2015 AHA Guidelines release. Great pick up!

We are wondering if the reason for listing hypothermia as a contraindication in general for symptomatic bradycardia is that severely hypothermic patients tend to be bradycardic and relatively hypotensive. In these clinical scenarios, it may be a superior strategy to treat the underlying cause (hypothermia) rather than perhaps making the hypothermic myocardium more irritable with Atropine or TCP. That being said, this does not explain the exemption (if you will) of Dopamine using the same argument.

As for your point about the practice of not giving drugs to the severely hypothermic patients, the 2010 AHA Guidelines (Vanden Hoek et al, Part 12: Cardiac Arrest in Special Situations) states the following for the management of the severely hypothermic patient on page S846:

ACLS management of cardiac arrest due to hypothermia focuses on aggressive active core rewarming techniques as the primary therapeutic modality. Conventional wisdom indicates that the hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation; however, the data to support this are essentially theoretical. In addition, drug metabolism may be reduced, and there is a theoretical concern that medications could accumulate to toxic levels in the peripheral circulation if given repeatedly to the severely hypothermic victim. For these reasons, previous guidelines suggest withholding IV drugs if the victim’s core body temperature is <30°C (86°F).

In the last decade a number of animal investigations have been performed evaluating both vasopressors and antiarrhythmic medications that could challenge some of this conventional wisdom. In a meta-analysis of these studies, Wira et al found that vasopressor medications (ie, epinephrine or vasopressin) increased rates of return of spontaneous circulation (ROSC) when compared with placebo (62% versus 17%; P<0.0001, n=77). Coronary perfusion pressures were increased in groups that received vasopressors compared with placebo. But groups given antiarrhythmics showed no improvement in ROSC when compared with control groups, although sample sizes were relatively small (n=34 and n=40, respectively).

One small-animal investigation suggested that the application of standard normothermic ACLS algorithms using both drugs (ie, epinephrine and amiodarone) and defibrillation improved ROSC compared with a placebo arm of defibrillation only (91% versus 30%; P<0.01; n=21). Human trials of medication use in accidental hypothermia do not exist, although case reports of survival with use of intra-arrest medication have been reported.

Given the lack of human evidence and relatively small number of animal investigations, the recommendation for administration or withholding of medications is not clear. It may be reasonable to consider administration of a vasopressor during cardiac arrest according to the standard ACLS algorithm concurrent with rewarming strategies (Class IIb, LOE C).

In other words, it may be reasonable to continue giving medications to profoundly hypothermic patients in the setting of cardiac arrest or cardiovascular collapse as long as we do so along with aggressive rewarming strategies. Since invasive active core rewarming is available in-hospital, this is why there continues to be a focus of early rapid transport as well with these patients.

Thanks again for the terrific question!

The relevant references from the AHA for this section are listed below:

Question: If TCP with Zoll E series, what are the steps to be taken when transferring care to the receiving facility? Procedure to switch to their machine?

Answer: It is difficult to answer this question given the regional nature of our program and the variability of receiving emergency departments’ equipment and the direction of the receiving emergency physicians. Our recommendation is when transferring care of transcutaneously paced patients communicate clearly with the receiving medical staff and ask for direction as to the sequence they prefer on a case by case basis to ensure that these unstable patients do not lose mechanical capture.

Question: On page 2-29 it says "A single dose of atropine should be considered for second degree type II or third degree AV blocks with fluid bolus”. Does that mean fluid bolus for both or just third degree?

Answer: A single dose of atropine should be considered for second degree Type II or third degree AV blocks with fluid bolus while preparing for TCP OR if there is a delay in implementing TCP OR if TCP is unsuccessful. Our intent is that a fluid bolus can be administered for both second degree Type II or third degree as described above. This came from a review of multiple cases over years of this clinical situation by one of the Regional Base Hospitals and they showed that the vast majority of these patients responded to this combination during the pre hospital phase. This is unpublished quality assurance data